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Stephen Safe - One of the best experts on this subject based on the ideXlab platform.

  • Estrogen Regulation of vascular endothelial growth factor gene expression in ZR-75 breast cancer cells through interaction of Estrogen receptor α and SP proteins
    Oncogene, 2003
    Co-Authors: Matthew Stoner, Mark Wormke, Brad Saville, Ismael Samudio, Chunhua Qin, Maen Abdelrahim, Stephen Safe
    Abstract:

    Estrogen Regulation of vascular endothelial growth factor gene expression in ZR-75 breast cancer cells through interaction of Estrogen receptor α and SP proteins

  • Estrogen Regulation of cyclin d1 gene expression in zr 75 breast cancer cells involves multiple enhancer elements
    Journal of Biological Chemistry, 2001
    Co-Authors: Emely Castrorivera, Ismael Samudio, Stephen Safe
    Abstract:

    Abstract Cyclin D1 gene expression is induced by 17β-estradiol (E2) in human breast cancer cells and is important for progression of cells through the G1 phase of the cell cycle. The mechanism of activation of cyclin D1 is mitogen- and cell context-dependent, and this study describes the role of multiple promoter elements required for induction of cyclin D1 by E2 in Estrogen receptor (ER)-positive ZR-75 breast cancer cells. Transcriptional activation of cyclin D1 by E2 was dependent, in part, on a proximal cAMP-response element at −66, and this was linked to induction of protein kinase A-dependent pathways. These results contrasted to a recent report showing that induction of cyclin D1 by E2 in ER-positive MCF-7 and HeLa cells was due to up-Regulation of c-jun and subsequent interaction of c-Jun-ATF-2 with the CRE. Moreover, further examination of the proximal region of the cyclin D1 promoter showed that three GC-rich Sp1-binding sites at −143 to −110 were also E2-responsive, and interaction of ERα and Sp1 proteins at these sites was confirmed by electromobility shift and chromatin immunoprecipitation assays. Thus, induction of cyclin D1 by E2 in ZR-75 cells is regulated through nuclear ERα/Sp1 and epigenetic protein kinase A activation pathways, and our results suggest that this mechanism may be cell context-dependent even among ER-positive breast cancer cell lines.

Ismael Samudio - One of the best experts on this subject based on the ideXlab platform.

  • Estrogen Regulation of vascular endothelial growth factor gene expression in ZR-75 breast cancer cells through interaction of Estrogen receptor α and SP proteins
    Oncogene, 2003
    Co-Authors: Matthew Stoner, Mark Wormke, Brad Saville, Ismael Samudio, Chunhua Qin, Maen Abdelrahim, Stephen Safe
    Abstract:

    Estrogen Regulation of vascular endothelial growth factor gene expression in ZR-75 breast cancer cells through interaction of Estrogen receptor α and SP proteins

  • Estrogen Regulation of cyclin d1 gene expression in zr 75 breast cancer cells involves multiple enhancer elements
    Journal of Biological Chemistry, 2001
    Co-Authors: Emely Castrorivera, Ismael Samudio, Stephen Safe
    Abstract:

    Abstract Cyclin D1 gene expression is induced by 17β-estradiol (E2) in human breast cancer cells and is important for progression of cells through the G1 phase of the cell cycle. The mechanism of activation of cyclin D1 is mitogen- and cell context-dependent, and this study describes the role of multiple promoter elements required for induction of cyclin D1 by E2 in Estrogen receptor (ER)-positive ZR-75 breast cancer cells. Transcriptional activation of cyclin D1 by E2 was dependent, in part, on a proximal cAMP-response element at −66, and this was linked to induction of protein kinase A-dependent pathways. These results contrasted to a recent report showing that induction of cyclin D1 by E2 in ER-positive MCF-7 and HeLa cells was due to up-Regulation of c-jun and subsequent interaction of c-Jun-ATF-2 with the CRE. Moreover, further examination of the proximal region of the cyclin D1 promoter showed that three GC-rich Sp1-binding sites at −143 to −110 were also E2-responsive, and interaction of ERα and Sp1 proteins at these sites was confirmed by electromobility shift and chromatin immunoprecipitation assays. Thus, induction of cyclin D1 by E2 in ZR-75 cells is regulated through nuclear ERα/Sp1 and epigenetic protein kinase A activation pathways, and our results suggest that this mechanism may be cell context-dependent even among ER-positive breast cancer cell lines.

Donald W. Pfaff - One of the best experts on this subject based on the ideXlab platform.

  • Estrogenic Regulation of gene and protein expression within the amygdala of female mice
    Endocrine, 2007
    Co-Authors: Aaron M. Jasnow, Jessica A. Mong, Russell D. Romeo, Donald W. Pfaff
    Abstract:

    Estrogens exert important actions on fear and anxiety in both humans and non-humans. Currently, the mechanisms underlying Estrogenic modulation of fear are not known. However, evidence suggests that Estrogens may exert their influence on fear and anxiety within the amygdala. The purpose of the present study was to examine the genomic effects of Estrogens within the amygdala of female mice using high-density oligonucleotide microarrays. We examined the effects of Estrogens on gene expression at 2 and 24 h after an acute subcutaneous injection. Data from the microarrays revealed that 2 h following an acute injection of estradiol, 44 genes were significantly up- or downregulated, and at 24 h, 13 transcripts were significantly up- or downregulated. One interesting Estrogen-regulated gene, (CaMKIIα), was downregulated ninefold 2 h following an acute estradiol injection but was not altered 24 h after injection. We further examined Estrogen Regulation of CaMKIIα, as well as CaMKIIβ and CaMKIV within the amygdala using quantitative PCR and western blot analysis. The data indicate that Estrogen decreases CaMKIIα and CaMKIV but not CaMKIIβ gene expression within the amygdala. However, CaMKII protein levels were not different, and CaMKIV protein levels increased 2 h post-EB treatment. These results indicate that Estrogen regulates CaMK gene expression and protein levels within the amygdala.

  • Estrogen Regulation of μ-opioid receptor mRNA in the forebrain of female rats
    Molecular Brain Research, 1997
    Co-Authors: Vanya Quiñones-jenab, Shirzad Jenab, Sonoko Ogawa, Charles E. Inturrisi, Donald W. Pfaff
    Abstract:

    Previous studies have suggested that opioids play a role in the Regulation of reproductive behaviors in the female rat. The present study examined whether Estrogen treatment alters mu-opioid receptor mRNA levels in different areas of the forebrain of ovariectomized (OVX) female rats using the in situ hybridization technique. We observed an increase in mu-opioid receptor mRNA levels in the ventromedial nucleus of the hypothalamus (VMH) and arcuate nucleus (ARN) after 48 h of 10 microg of 17-beta-estradiol-3-benzoate treatment when compared to OVX females. No effects of Estrogen were observed on mu-opioid receptor mRNA levels in the posterior medial nucleus of the amygdala (MeAmyg), hippocampus, caudate-putamen (CPu) or the medial habenula. Our result suggests that the Estrogenic Regulation of mu-opioid receptor in the CNS may in part be mediated by de novo synthesis and/or stability of the mu-opioid receptor message.

  • Estrogen Regulation of gonadotropin-releasing hormone receptor messenger RNA in female rat pituitary tissue
    Molecular Brain Research, 1996
    Co-Authors: Vanya Quiñones-jenab, Shirzad Jenab, Sonoko Ogawa, Toshiya Funabashi, Gary D. Weesner, Donald W. Pfaff
    Abstract:

    Gonadotropin releasing hormone (GnRH) is crucial in regulating the reproductive system of female vertebrates. In the present study we have analyzed the Estrogen Regulation of the GnRH receptor mRNA at the cellular level in Sprague-Dawley female rats. Northern blot analysis detected 3 species (5.0, 4.5 and 1.4 kb) of GnRH receptor mRNA in pituitary tissues. The GnRH receptor mRNA levels of these 3 species were increased by Estrogen. By in situ hybridization we observed a 3.5-fold increase in GnRH receptor mRNA levels after 48 h of Estrogen treatment when compared to ovariectomized (OVX) rats, 12 h of Estrogen treatment did not change the GnRH mRNA levels. Similar increases in GnRH receptor mRNA levels by Estrogen were also found in Wistar-Imamichi female rat pituitary tissue. In situ hybridization analysis identified clusters of anterior pituitary cells that expressed the GnRH receptor mRNA. The estradiol effect depends on increased mRNA levels in these clusters. Moreover, a significant increase in the number of pituitary cells that expressed GnRH receptor was observed after 48 h of Estrogen treatment. These findings suggest that the mechanisms for Estrogen Regulation of GnRH receptor include changing levels of GnRH receptor mRNA in the rat pituitary.

  • behavioral aspects of neuroendocrinology
    1991
    Co-Authors: Detlev Ganten, Donald W. Pfaff, H A Baldwin
    Abstract:

    Behavioral Effects of Corticotropin-Releasing Factor.- Corticotropin-Releasing Factor: Central Regulation of Autonomic Nervous and Visceral Function.- Oxytocin as Part of Stress Responses.- Behavioral Effects of Vasopressin.- Neuropeptide Control of Parental and Reproductive Behavior.- Estrogen Regulation of mRNAs in the Brain and Relationship to Lordosis Behavior.- The Neuroendocrinology of Thirst: Afferent Signaling and Mechanisms of Central Integration.- Neuropeptide Y: A Novel Peptidergic Signal for the Control of Feeding Behavior.- Neuropeptide Mechanisms Affecting Temperature Control.- Cytokines and Sleep.- Behavioral Effects of Prolactin.

Jerome Eeckhoute - One of the best experts on this subject based on the ideXlab platform.

  • differential Estrogen Regulation of cxcl12 chemokine receptors cxcr4 and cxcr7 contributes to the growth effect of Estrogens in breast cancer cells
    PLOS ONE, 2011
    Co-Authors: Antoine Boudot, Jerome Eeckhoute, Gwenneg Kerdivel, Denis Habauzit, Francois Le Dily, Gilles Flouriot, Michel Samson, Farzad Pakdel
    Abstract:

    CXCR4 and CXCR7 are the two receptors for the chemokine CXCL12, a key mediator of the growth effect of Estrogens (E2) in Estrogen receptor (ER)-positive breast cancers. In this study we examined E2-Regulation of the CXCL12 axis components and their involvement in the growth of breast cancer cells. CXCR4 and CXCR7 were differentially regulated by E2 which enhanced the expression of both CXCL12 and CXCR4 but repressed the expression of CXCR7. Formaldehyde-associated isolation of regulatory elements (FAIRE) revealed that E2-mediated transcriptional Regulation of these genes is linked to the control of the compaction state of chromatin at their promoters. This effect could be accomplished via several distal ER-binding sites in the regions surrounding these genes, all of which are located 20–250 kb from the transcription start site. Furthermore, individual down-Regulation of CXCL12, CXCR4 or CXCR7 expression as well as the inhibition of their activity significantly decreases the rate of basal cell growth. In contrast, E2-induced cell growth was differentially affected. Unlike CXCR7, the inhibition of the expression or activity of either CXCL12 or CXCR4 significantly blunted the E2-mediated stimulation of cellular growth. Besides, CXCR7 over-expression increased the basal MCF-7 cell growth rate and decreased the growth effect of E2. These findings indicate that E2 Regulation of the CXCL12 signaling axis is important for the E2-mediated growth effect of breast cancer cells. These data also provide support for distinct biological functions of CXCR4 and CXCR7 and suggest that targeting CXCR4 and/or CXCR7 would have distinct molecular effects on ER-positive breast tumors.

  • a cell type specific transcriptional network required for Estrogen Regulation of cyclin d1 and cell cycle progression in breast cancer
    Genes & Development, 2006
    Co-Authors: Jerome Eeckhoute, Maria I Torresarzayus, Timothy R Geistlinger, Jason S. Carroll, Myles Brown
    Abstract:

    Estrogen stimulates the proliferation of the most common type of human breast cancer that expresses Estrogen receptor α (ERα) through the activation of the cyclin D1 (CCND1) oncogene. However, our knowledge of ERα transcriptional mechanisms remains limited. Hence, it is still elusive why ERα ectopically expressed in ER-negative breast cancer cells (BCC) is functional on ectopic reporter constructs but lacks activity on many endogenous target genes, including CCND1. Here, we show that estradiol (E2) stimulation of CCND1 expression in BCC depends on a novel cell-type-specific enhancer downstream from the CCND1 coding region, which is the primary ERα recruitment site in Estrogen-responsive cells. The pioneer factor FoxA1 is specifically required for the active chromatin state of this enhancer and as such is crucial for both CCND1 expression and subsequent cell cycle progression. Interestingly, even in BCC, CCND1 levels and proliferation are tightly controlled by E2 through the establishment of a negative feedforward loop involving the induction of NFIC, a putative tumor suppressor capable of directly repressing CCND1 transcription. Taken together, our results reveal an Estrogen-regulated combinatorial network including cell-specific cis- and trans-regulators of CCND1 expression where ERα collaborates with other transcription factors associated with the ER-positive breast cancer phenotype, including FoxA1 and NFIC.

Caterina Faggio - One of the best experts on this subject based on the ideXlab platform.

  • Estrogen Regulation of gene expression in the teleost fish immune system
    Fish & Shellfish Immunology, 2016
    Co-Authors: Mario Alberto Burgosaceves, Amit Cohen, Yoav Smith, Caterina Faggio
    Abstract:

    Elucidating the mechanisms of Estrogens-induced immunomodulation in teleost fish is of great importance due to the observed worldwide continuing decrease in pristine environments. However, little is know about the immunotoxicological consequences of exposure to these chemicals in fish, or of the mechanisms through which these effects are mediated. In this review, we summarize the results showing Estrogens (natural or synthetic) acting through Estrogen receptors and regulating specific target genes, also through microRNAs (miRNAs), leading to modulation of the immune functioning. The identification and characterization of miRNAs will provide new opportunities for functional genome research on teleost immune system and can also be useful when screening for novel molecule biomarkers for environmental pollution.